ADENOSINE is a potent modulator of transmitter release at a variety of synapses. The adenosine Al receptor is assumed to reside in presynaptic terminals and to function as a negative autoreceptor1. How adenosine reduces transmitter release is uncertain2; it may reduce the calcium influx during nerve terminal depolarization by either activating K+ currents3,4 or inhibiting Ca2+ currents5,6, although other mechanisms have been proposed7-9. We have directly measured intracellular Ca2+ concentrations of giant presynaptic terminals in the chick ciliary ganglion. We report here that adenosine inhibited the nerve-evoked Ca2+ influx in the termi-nal by activating Al receptors. Reduced Ca2+ influx was due largely to inhibition of ω-conotoxin GVIA-sensitive Ca2 + channels in the presynaptic terminal.
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